Effect of a 12-Week Rehabilitation Exercise Program on Shoulder Proprioception, Instability and Pain in Baseball Players with Shoulder Instability.

BACKGROUND: The shoulder joint has a wide range of motion, but is vulnerable to sport-related injuries. We aimed to evaluate the differences in the proprioception of the shoulder should instability, and shoulder pain in high school baseball players with shoulder instability following a 12-week rehabilitation exercise program. METHODS: We enrolled 13 baseball players with shoulder instability who visited the Orthopedics Department at Konkook University Hospital in Seoul, South Korea and 12 controls without shoulder instability. We examined the dominant shoulder and the non-dominant shoulder for both groups. We restricted participation to individuals who had no other orthomechanical disease in the past six months, except for instability of the shoulder, and no physical limitation to participate in the exercise. We measured the proprioception of the shoulder and shoulder instability, and we also evaluated pain with the Visual Analog Scale before and after the rehabilitation program. To verify the differences between groups, we used a two-way analysis of variance, and a two-way analysis of covariance was used when a significant difference was found at the pretest (baseline between groups). RESULTS: Proprioception was associated with shoulder instability. The Visual Analog Scale rating improved in the dominant shoulder with instability; and a positive change was found in the dominant shoulder without instability after the rehabilitation program (P < 0.05). CONCLUSION: The 12-week rehabilitation exercise program might improve the proprioception and pain of patients with shoulder instability. However, further studies with more participants and a rehabilitation exercise program should be undertaken.

Nitric oxide and interleukin-1ß stimulate the proteasome-independent degradation of the retinoic acid hydroxylase CYP2C22 in primary rat hepatocytes.

CYP2C22 was recently described as a retinoic acid-metabolizing cytochrome P450 enzyme whose transcription is induced by all-trans-retinoic acid (atRA) in hepatoma cells (Qian L, Zolfaghari R, and Ross AC (2010) J Lipid Res 51:1781-1792). We identified CYP2C22 as a putative nitric oxide (NO)-regulated protein in a proteomic screen and raised specific polyclonal antibodies to CYP2C22 to study its protein expression. We found that CYP2C22 is a liver-specific protein that was not significantly induced by activators of the pregnane X receptor, constitutive androstane receptor, or peroxisome proliferator-activated receptor-α, but was downregulated to <25% of control by the aryl hydrocarbon receptor agonist ß-naphthoflavone in cultured rat hepatocytes. CYP2C22 protein and its mRNA both were induced by atRA in hepatocytes, with EC50 of 100-300 nM, whereas the maximal extent of mRNA induction was twice that of the protein. CYP2C22 protein, but not its mRNA, was rapidly downregulated in hepatocytes by interleukin-1 (IL-1) or NO-donating compounds, and the downregulation by IL-1 was blocked by inhibition of NO synthases. The NO donor (Z)-1-[N-(3-aminopropyl)-N-(3-ammoniopropyl)amino]diazen-1-ium-1,2-diolate reduced the half-life of CYP2C22 from 8.7 to 3.4 hours in the presence of cycloheximide, demonstrating that NO-dependent downregulation is due to stimulated proteolysis. No intermediate degradation products were detected. However, this degradation was insensitive to inhibitors of calpains or the canonical proteasomal or lysosomal pathways, indicating that NO-dependent degradation of CYP2C22 proceeds via a novel pathway.